Release of 15-keto-13, 14-dihydro-thromboxane B2 and prostaglandin D2 during anaphylaxis as measured by radioimmunoassay

1978 ◽  
Vol 305 (3) ◽  
pp. 247-252 ◽  
Author(s):  
H. Anhut ◽  
B. A. Peskar ◽  
W. Bernauer
Keyword(s):  
Thromboxane B2 ◽  
Prostaglandin D2

scholarly journals Effects of Pyrazolone Drugs on Synthesis of Prostaglandin D2 and Thromboxane B2 by Platelets

1977 ◽  
Author(s):  
M. Ali ◽  
J. Zamecnik ◽  
J. W. D. McDonald
Keyword(s):  
Mass Spectrometry ◽  
Human Platelets ◽  
Thromboxane B2 ◽  
Gas Chromatography Mass Spectrometry ◽  
Prostaglandin D2 ◽  
Freezing And Thawing ◽  
Plasma Albumin ◽  
Cyclooxygenase Activity ◽  
Silicic Acid Chromatography ◽  
Hydroxylated Fatty Acids

The principle products of arachidonic acid (AA) in platelets are hydroxylated fatty acids and thromboxane B2(TXB2). Prostaglandin D2(PGD2) has been considered to be a nonenzymatic degradation product of prostaglandin H2 formed in the presence of plasma albumin. Using 14C AA as substrate and thin layer and silicic acid chromatography, we have demonstrated PGD2 synthesis by washed (albumin-free) human platelets. The identity of PGD2 was confirmed by gas chromatography-mass spectrometry. In platelets lysed by freezing and thawing synthesis of TXB2 and PGD2 was approximately equal and equally inhibited by pyrazolones.Synthesis of PGD2 by platelets is enzymatic and may contribute to bronchoconstrictor, vasomotor, and inflammatory effects induced by platelet aggregation. Pyrazolones appear to inhibit cyclooxygenase activity rather than the breakdown of cyclic endoperoxides as previously postulated.

scholarly journals Stimulation of release of prostaglandin D2 and thromboxane B2 from perfused rat liver by extracellular adenosine

1990 ◽  
Vol 270 (1) ◽  
pp. 39-44 ◽  
Author(s):  
S vom Dahl ◽  
M Wettstein ◽  
W Gerok ◽  
D Häussinger
Keyword(s):  
Rat Liver ◽  
Portal Pressure ◽  
Thromboxane B2 ◽  
Adenosine Infusion ◽  
Isolated Perfused Rat Liver ◽  
Signal Molecules ◽  
Prostaglandin D2 ◽  
Perfused Rat Liver ◽  
Glucose Output ◽  
Stimulation Of

In isolated perfused rat liver, adenosine infusion (50 microM) led to increases in glucose output and portal pressure and a net K+ release of 3.7 +/- 0.21 mumol/g, which was followed by an equivalent net K+ uptake after cessation of the nucleoside infusion. These effects were accompanied by a transient stimulation of hepatic prostaglandin D2 and thromboxane B2 release. The Ca2+ release observed upon adenosine infusion (50 microM) was 23.5 +/- 5.2 nmol/g, i.e. 10-20% of the Ca2+ release observed with extracellular ATP (50 microM). Indomethacin (10 microM) prevented the adenosine-induced stimulation of glucose output and the increase in portal pressure by 79 and 63% respectively, and completely abolished the stimulation of prostaglandin D2 release. The thromboxane A2 receptor antagonist BM 13.177 (20 microM), the phospholipase A2 inhibitor 4-bromophenacyl bromide (20 microM) and the cyclo-oxygenase inhibitor ibuprofen (50 microM) also decreased the glycogenolytic and vasoconstrictive responses of the perfused rat liver upon adenosine infusion by 50-80%. When the indomethacin inhibition of adenosine-induced prostaglandin D2 release was titrated, a close correlation between prostaglandin D2 release and the metabolic and vascular responses to adenosine was observed. These findings suggest an important role for eicosanoids in mediating the nucleoside responses in the perfused rat liver. Since eicosanoids are known to be formed by non-parenchymal cells in rat liver [Decker (1985) Semin. Liver Dis. 5, 175-190], the present study gives further evidence for an important role of eicosanoids as signal molecules between the different liver cell populations.

Synthesis of prostaglandin D2 and thromboxane B2 by human platelets

1977 ◽  
Vol 11 (4) ◽  
pp. 485-496 ◽  
Author(s):  
M. Ali ◽  
A.L. Cerskus ◽  
J. Zamecnik ◽  
J.W.D. McDonald
Keyword(s):  
Human Platelets ◽  
Thromboxane B2 ◽  
Prostaglandin D2

scholarly journals Melittin stimulates liver glycogenolysis and the release of prostaglandin D2 and thromboxane B2

1990 ◽  
Vol 269 (1) ◽  
pp. 273-275 ◽  
Author(s):  
J A García-Sáinz ◽  
S M T Hernández-Sotomayor ◽  
M Macías-Silva
Keyword(s):  
Rat Liver ◽  
Thromboxane B2 ◽  
Prostaglandin D2 ◽  
Perfused Rat Liver ◽  
Initial Burst ◽  
Glucose Output ◽  
Liver Glycogenolysis ◽  
Stimulation Of

Melittin stimulates glycogenolysis and induces vasoconstriction in perfused rat liver. The effect was rapid and associated with production and release of prostaglandin D2 and thromboxane B2. Indomethacin blocked the release of these eicosanoids and the stimulation of glycogenolysis induced by melittin. Ibuprofen blocked the release of prostaglandin D2 induced by melittin and markedly attenuated that of thromboxane B2. Interestingly, the initial burst of glucose output induced by melittin was not inhibited by ibuprofen, although the duration of the glycogenolytic action of the peptide was greatly diminished.

scholarly journals Hepatocyte heterogeneity in response to extracellular adenosine

1993 ◽  
Vol 293 (2) ◽  
pp. 573-581 ◽  
Author(s):  
Y Morimoto ◽  
M Wettstein ◽  
D Häussinger
Keyword(s):  
Perfusion Pressure ◽  
Thromboxane B2 ◽  
Prostaglandin D2 ◽  
Extracellular Adenosine ◽  
Single Pass ◽  
Prostaglandin Release ◽  
Adenosine Concentration ◽  
Hepatocyte Heterogeneity ◽  
Glucose Output ◽  
Eicosanoid Formation

Metabolic and haemodynamic effects of adenosine were studied in antegrade and retrograde rat liver perfusions with influent nucleoside concentrations either below (i.e. 20 microM) or exceeding (i.e. 200-300 microM) the single-pass clearance capacity of the liver. Adenosine (20 microM) increased in antegrade perfusions the perfusion pressure and markedly stimulated prostaglandin D2, thromboxane B2 and glucose output, whereas in retrograde perfusions no pressure and eicosanoid response occurred and glucose output was stimulated only slightly. The perfusion-direction-dependent differences in the glucose and pressure response to adenosine (20 microM) were fully abolished in presence of ibuprofen (50 microM). When the adenosine concentration in influent was raised to 200-300 microM, i.e. to a concentration exceeding single-pass clearance of the nucleoside, the adenosine-induced prostaglandin D2 release was about 10-fold higher in retrograde perfusions than in antegrade perfusions. On the other hand, both adenosine (20-300 microM)-induced cyclic AMP (cAMP) and K+ release from the liver were not affected by the direction of perfusion, and maximal effects on cAMP release were observed at influent adenosine concentrations of 100 microM. The basal rate (adenosine absent) of prostaglandin D2 and thromboxane B2 release was about 10-fold higher in retrograde than in antegrade perfusion experiments, whereas the basal cAMP release from the liver was not affected by the direction of perfusion. Maximal adenosine-stimulated glucose output was significantly higher in antegrade than in retrograde perfusions at all adenosine concentrations tested (range 10-300 microM). Ibuprofen abolished this difference, indicating that eicosanoids liberated under the influence of adenosine contribute to the glycogenolytic response in antegrade, but not in retrograde, perfusion. Desensitization occurred following repetitive adenosine infusion; this was more pronounced for adenosine-induced prostaglandin release than for cAMP or K+ efflux. The data suggest the following. (i) Both cAMP and eicosanoids are involved in the stimulation of glycogenolysis by adenosine. (ii) Eicosanoids are probably liberated under the influence of extracellular adenosine from a portal pre-sinusoidal compartment and accordingly stimulate glycogenolysis only in antegrade perfusions. Thus signals derived from portal vein structures can modulate hepatocellular function. (iii) Contractile elements are probably located also inside the liver acinus. (iv) Eicosanoids released into the hepatic vein reflect less than 10% of hepatic eicosanoid formation, because of marked clearance by perivenous hepatocytes.

scholarly journals YC-1, a novel activator of platelet guanylate cyclase

Blood ◽  
1994 ◽  
Vol 84 (12) ◽  
pp. 4226-4233 ◽  
Author(s):  
FN Ko ◽  
CC Wu ◽  
SC Kuo ◽  
FY Lee ◽  
CM Teng
Keyword(s):  
Sodium Nitroprusside ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Intraperitoneal Administration ◽  
Thromboxane B2 ◽  
Prostaglandin D2 ◽  
Dependent Manner ◽  
Camp Phosphodiesterase ◽  
Concentration Dependent Manner ◽  
Rabbit Platelets

YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole] inhibited the aggregation of and ATP release from washed rabbit platelets induced by arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF), and thrombin in a concentration-dependent manner. YC-1 also disaggregated the clumped platelets caused by these inducers. The thromboxane B2 formation caused by collagen, PAF, and thrombin was inhibited by concentrations of YC-1 that did not affect formation of thromboxane B2 and prostaglandin D2 caused by AA. YC-1 suppressed the increase of intracellular Ca2+ concentration and generation of inositol 1,4,5-trisphosphate caused by these five aggregation inducers. Both the cAMP and cGMP contents of platelets were increased by YC-1 in a concentration- and time-dependent manner. Like sodium nitroprusside, YC- 1 potentiated formation of cAMP caused by prostaglandin E1 but not that by 3-isobutyl-1-methylxanthine. Adenylate cyclase and cAMP phosphodiesterase activities were not altered by YC-1. Activity of cGMP phosphodiesterase was unaffected by YC-1. Activities of guanylate cyclase in platelet homogenate and cytosolic fraction were activated by YC-1, whereas particulate guanylate cyclase activity was unaffected. The antiplatelet effect of sodium nitroprusside but not that of YC-1 was blocked by hemoglobin and potentiated by superoxide dismutase. After intraperitoneal administration for 30 minutes, YC-1 prolonged the tail bleeding time of conscious mice. These data indicate that YC-1 is a direct soluble guanylate cyclase activator in rabbit platelets. It may also possess antithrombotic potential in vivo.

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